Our study has identified the CCL2/CCR2-STAT3-EMT axis as potential new targets to improve the clinical outcome of PCa patients under ADT, and combination therapy of targeting AR and anti-CCL2/CCR2 (and also probably its downstream mediator, STAT3) might help us to better battle PCa at the castration resistant stage. The gene discussed is CCR2; the disease is posterior cortical atrophy.